Discover more from Harvard to The Big House - Straight to Your House
Golden Silkworms in Pandora's Box
Why understanding COVID-19 and Seasonal Influenza as Quasispecies Swarms reveals the Quantum Origins and Cryptic Fates of Human Pandemics.
From the co-author of the first peer-reviewed paper examining a laboratory origin for SARS-CoV-2, as well as its addendum, which formally linked the H1N1 Spanish Flu pandemic strain release of 1977 to gain-of-function research.
What happens when dangerous and unproven scientific research techniques meet the military-industrial complex? Are modern research scientists still controlled by any code of ethics at all?
Is the COVID-19 Pandemic an inevitable product of the “Publish-or-Perish” mentality that’s turning both academia and popular journalism into factory farms whose primary goal is monetization – not the public good?
Answering these questions will reveal the ties that bind together the histories of mysterious military illnesses, the emergence of HIV, the source of the 1918 Spanish Flu Pandemic, anal swabs, COVID-19’s origins, Original Antigenic Sin, both the SARS and MERS Outbreaks, the 2009 Swine Flu Pandemic, as well as experimental but profitable vaccination protocols – all to the fates of those who would put fame and fortune over human life and academic ethics.
SPOILER ALERT: SARS-CoV-2 is a circulating vaccine-derived-coronavirus (cVDCV) borne from work originally done at UNC, the only institution on earth that’s publicly been attempting to design a live-attenuated vaccine for SARS, where they also pioneered engineering the SARS-like chimeric coronaviruses that would be needed as templates for attenuation, and did their best to ignore or circumvent restrictions on gain-of-function research – obfuscation that’s still ongoing as they refuse to disclose genomic details relating to lab accidents that occurred during the above publicly-funded research.
Notorious researchers from the Wuhan Institute of Virology were associated with this controversial work on coronaviruses, and attempted to continue it with an experimental oral live-attenuated SARS-like vaccination program for the Chinese Military without accounting for the quantum nature of the underlying quasispecies behavior – once they realized what was going on and deattenuation was already occurring out-of-control after the Wuhan Military Games, they reopened contact with Dr. Charles Lieber due to his work on virus-distinguishing nanowires, eventually leading to his arrest and the beginning of the largest and most coordinated cover-up in world history.
Carried-out by the pharmaceutical and defense entities involved in this research, both of which want attention pulled away from serial passage and experimental vaccine work, as do the billionaire class that wants to use gain-of-function research for unrestricted tinkering into the human genome at the Broad Institute.
Tale as old as time, death as old as rhyme: When the rich play God, it’s the poor who die.
Part I – Monkeys and Manias.
Few things are more terrifying than being an exhausted fat kid about three-quarters of the way into your first 5k cross-country race when it’s being hosted at Fort Detrick, and you spent the previous night reading about the possibility of Ebola-infected monkeys escaping from military research facilities just like this one - potentially setting off a global pandemic as depicted in The Hot Zone.
So as the last few hundred yards go into a gully stretching past fencing that's ominously topped with several rows of concertina wire, and your left calf starts cramping right as something rustles angrily towards you in the overgrowth behind the fence, you realize that you can in fact keep going after you think you feel the hot hungry breathe of a pandemically diseased lab monkey growing closer - ready to bite you and start an infection that results in blood violently fountaining out of your mouth and anus like some kind of terrible reverse-hemorrhagic Chinese-fingercuffs, uncontrollably spraying nearby runners with the disease and seeding a global pandemic and the death of millions.
Even for a fat kid, that’d be a heavy burden to bear, and so you keep running until you reach the finish line, glancing over your shoulder as you collapse into the grass to make sure no Ebola-crazed simians are after you. But the good news about finishing a cross-country race in last place is it means no one else is coming - definitely no escaped monkeys, and so it seems safe to forget about escaped lab animals and pandemics, at least for a little while.
Most kids of the past couple generations growing up with a parent involved with scientific research were probably more aware than most of their friends about the plight of lab animals, since at some point watching The Secrets of NIMH probably got you thinking about the suffering that can be shared by all intelligent creatures. But then a few years later, the Teenage Mutant Ninja Turtles likely put a lighter spin on the whole idea, and you don’t worry about technological progress so much. And then maybe later on down the road there was some exposure to factory farming, a different side of the same industrialized hyper-populated coin, and some dabbling in vegetarianism until the smell at the National Capitol Barbeque just became too much.
However at some point you realize that modern civilization doesn’t happen without humans bending Nature to our will as much as we possibly can, in a way that’s a defining characteristic of civilization itself, and you go about your life. Luckily for many of us, we were born into an era of modern medicine that’s demonstrated mankind’s inherent superiority over whatever Nature can throw at us, starting with plant domestication and animal husbandry forming the underpinnings of civilization itself, and continuing until today where farm animals are packed into once unimaginable densities, and laboratory animals are getting shanghaied into sprouting entire human organs to and having our genes spliced directly into them so they can be used for vaccines and other medical wonders.
But it turns out, under the wrong conditions, some the same principles which make the established childhood vaccination protocols so important and so safe can begin to rub up against the hubris of our modernity, and start to smolder. And when it begins to sense enough smoke, a very ancient miasma begins to unfurl from its slumber, soon noticing the burning hunger that’s been building since the last time we woke it up with our collective drive for domination and plunder.
The science underpinning modern medicine would’ve seemed like magic just a few generations ago, and even understanding the mechanisms behind many phenomena – it still often does. And yet modern science seems to have forgotten about one of the older lessons in magic, which was likely rooted in a fundamental understanding of the natural order of things: Nothing comes without its price.
Then in the latter part of 2019, a stark reminder of this natural balance would appear in Wuhan, China and soon spread to the rest of the world in the first recorded pandemic created by a coronavirus in human history. But to understand what it’s trying to tell us, it’s important to try and hear what it was trying to say the first few times around.
1. “We few, we happy few, we band of brothers.”
Although the speech this quote immediately elicits occurred a few decades before the War of the Roses, Shakespeare’s appropriation of it ensured that it would’ve been running through the souls of the soldiers fighting there just as it was during the Battle of Agincourt a few decades later. And although these words were addressed to English troops, these conflicts documented for the first time that there was a much more influential and mysterious band of brothers on the battlefield besides the ones doing the fighting - as the emergence of a bizarre illness was used by one of the English Lords as a reason to pull out of the battle shortly before it began, almost certainly changing the tide of the entire war, and all of our shared history.
1485 marked a temporary end to the successional struggle for England’s crown, but also the start of a series of five mysterious endemics that came to collectively be known as the English Sweat, which seemed to be heavily correlated with previous periods of heavy rainfall followed by intense human activity. By 1604 it had become such a ubiquitous force across England that the Bard mentioned it intentionally in another play, this time as a central force of social decay: “…what with the war, what with the sweat, what with the gallows, and what with poverty.”
Part of the terror it inspired was due to its lethality, it would typically kill its victims within 24 hours – chills, tremors, fever, a rash, sweating, then the Reaper - and its mortality rate is generally agreed upon to have been somewhere between 30% and 50%. The second horrifying factor was its apparent genocidal intent – for reasons that have never been explained at all until now, the English Sweat got its nationality not only because that’s where it began, but because as many historical observers inquisitively noted: It only ever appeared to kill the English, every other nationality appeared to be spared while on English soil.
And since its outbreaks often began in direct correlation to war, other nations would call it “Military Fever” when it sparked up on their soil, the moniker it took as one of its more continental strains killed Mozart. This martial connection was an inescapable one to make, as this first outbreak followed the victorious army back to London, where it burnt across the public throngs gathered in the thousands around their barracks to celebrate the victory.
Then, during its 1508 occurrence, it would demonstrate an important demographic flashpoint as its embers would float across the English Channel and land at the Pas-de-Calais. Yet even here across the Channel and on French land, it would still only kill the English. Burning white-hot when it appeared, the English Sweat appeared in intervals of roughly either 10 or 20 years, not targeting the young and vulnerable or old and infirm like most diseases, but instead the “middle-aged, professionally active section of the population,” or those gathered in close quarters like the military and monks.
The English Sweat is the first modern record of a paradoxical immunological puzzle being linked to a military setting, but it certainly wasn’t the first disease, and wouldn’t be the last riddle.
1.1 War is a disease.
Human influenza can be traced with reasonable certainty back to the Trojan War over 3,000 years ago, the first time it appears to enter the historical record with any reliability. A millennium or so later around the time of the Late Bronze Age Collapse, smallpox would leave its scars on a mummified Pharaoh, and other diseases suspected to be tularemia and the plague would also ravage those ancient battlefields.
Once the Roman Empire emerged, its armies too eventually fell victim, along with the empire itself, to wave after wave of diseases. One of the most lethal, the Antonine Plague, was thought to have started during the siege of a Mesopotamian city and then spread across the entire Empire - likely smallpox or one of its close relatives helping bring another Empire into an early grave.
And over 500 years after the English Sweat emerged, the world’s militaries would still be battling disease as much as each other, and in 1954 the U.S. Navy and Marines would begin their influenza vaccination programs since the inescapably packed conditions of ocean-bound naval vessels made for giant Petri dishes, mimicking the conditions found on commercial farms – making an airborne pathogen like influenza the primary concern since by the 20th century, modern militaries and societies have largely learned to remove intermediate animal vectors like mice.
So in 1996 when the military noticed that the USS Arkansas suffered a serious outbreak of influenza that affected at least 42% of her crew despite the fact that 95% had been properly vaccinated prior to departure, scientists were left largely scratching their heads. All of their analysis seemed to indicate that the vaccine should have covered the strains that were circulating, and so there didn’t seem to be any answer as to why so many seamen got so sick.
However in the decades to come it’s the exact same puzzle that would be faced on densely packed poultry farms where influenza transmission is also inescapable, and its an answer that will unlock the origins of both the 1918 Spanish Flu as well as the COVID-19 Pandemic with a combination that involves the inevitable consequences of a world that grows continually more densely packed with humanity, and the never-ending push to develop new and improved experimental vaccines for profit and plunder.
Microbiology first took the world by storm in 1880 when Louis Pasteur demonstrated that it was microbes – invisible to the naked eye – which were responsible not only for the sickness and disease which haunted the poor and unfortunate, something no one really worried about too much, but also led to the destruction of silk and wine farms.
Now that luxury items were demonstrated to be targeted by microbes in addition to the poor, the world took notice - since now dollar signs could be placed on the science. Not for the first time, and certainly not the last.
Although it became a bit of a long road, Pasteur had stumbled across the theory of attenuation after he used some of the chicken cholera that he’d been using to basically just Mengele chickens to death with, which had been laying out exposed to the elements, to dose some chickens with, and then went on summer vacation. Returning to his lab, the chickens exposed to the weakened virus were the only leftover poultry, so by default he chose them for the first round of testing his full-strength strain of cholera against, and noticed that not only did they survive – they hardly even got sick.
Realizing that leaving the cholera out in the elements had effectively weakened it and allowed the chickens exposed to its weakened form to develop resistance to it without killing them, Pasteur coined the term “attenuation” to describe a lesser version of the process that took his name, of totally sterilizing something – Pasteurization. So it was attenuation, originally of the cholera bacteria, that allowed for bespoke live-attenuated vaccines (LAVs) to first be designed against bacteria and then against viruses. Prior to this, variolation could only offer protection against a virus if a safe close cousin was hosted by livestock like with cowpox and smallpox, but mastering attenuating LAVs opened the door to creating extremely effective vaccines for every single virus out there.
So although the scientific world took a fair amount of convincing, Pasteur eventually demonstrated the efficacy of his chicken cholera LAV, and would eventually devise an ingenious LAV against the rabies virus that was sent through rabbit cells to weaken it down, that could even be used post-exposure on both dogs and humans. Rabies was likely the easiest target to attenuate down into a LAV because it presents to often in its highly-pathogenic and zoonotic state, as the virus drives its host to the horribly hallmark of foamy madness that makes this highly-pathogenic state - which displays the full range of epitopes the immune system would need to learn to target - so easy to identify and get samples from. Other LAVs were either created from viruses that also naturally presented in their highly-pathogenic state, like the highly lethal strain of Yellow Fever used for its LAV, or would use multiple strains to mimic this state and present the full range of epitopes that way, the strategy taken against Polio.
And as fate would have, the very first life that revolutionary live-attenuated vaccine saved was of a little boy who would grow up to be the man who would refuse the Nazis entrance into Pasteur’s crypt, committing suicide fifty-five years after the scientist had saved his young life, in an attempt to keep his genius out of Nazi hands. But unfortunately for undesirables everywhere, the Nazis wouldn’t need Pasteur’s ideas to inflict levels of suffering that only the organization and mechanization of the industrial world could make possible, and during World War II the Japanese would use another pathogen Pasteur had devised a vaccine against – anthrax which the Japanese military first tested on POWs – to kill enemy troops for the first time, as the Chinese became the first victims of the modern age of intentionally-isolated biological warfare.
But back in 16th century England, it wouldn’t be until 1551, the start of its last endemic, that the English Sweat appears to have dissipated from history. The best guess scientists have come up with for its entire mysterious existence is that it was caused by a rodent-borne RNA virus known as a hantavirus that causes hemorrhagic fever, since rodents would’ve been expected to proliferate after heavy rainfall, can transmit hantaviruses through their wastes or bites, and the clinical presentations largely line up. However this is very much a guess, since nothing about hantaviruses – or any pathogen as they’re currently understood – can yet explain why only the English were targeted, nor the way isolated pockets of the diseases would flare up independently from each other, and then each endemic would burn with apparently random intensities of sickness and death, with no apparent pattern of transmission across time or location.
Although it would flare up at population centers, there was no evidence of anything resembling the steady and mostly linear transmission of a pathogen that would be expected from typical immunological modeling – especially not how it could possibly drift from England across the Channel at the Pas-de-Calais, and decide to only kill the Englishmen gathered there. Unfortunately, since genomic sequencing was still a few hundred years away, it’s unlikely we’ll ever know for certain where the English Sweat came from, or where it went.
However there’s a chance that if we stare hard enough into this historical miasma, we’ll be able to hear our future squeaking back at us.
2. “Appear weak when you are strong, and strong when you are weak.”
Although it was once considered eradicated, in recent years an increasing number of cases of poliomyelitis – polio’s terrible paralytic curse - have emerged in the developing world after remnants of the three highly attenuated Oral Polio Vaccine (OPV) live-attenuated virus strains used to inoculate children managed to escape into the population, circulating and mutating and deattenuating enough to eventually establish active human infections.
This novel global phenomenon would’ve been anticipated by the late U.S. Army Major Dr. Albert Sabin, who served in the Pacific Theater and designed the OPV-LAV protocol in the 1950s to compliment the inactivated vaccine which didn’t quite seem to be enough to fully eradicate the slippery disease. Dr. Sabin would’ve been well-aware of the risks involved with attempting to design a LAV against RNA viruses like Polio, since back in 1935 an experimental polio LAV had deattenuated back to full neurovirulence, and killed five of the several thousand children inoculated with it in Philadelphia.
So several years later in the 1950s, Sabin was careful to make sure the three strains he chose for his viral swarm would be unable to reassemble themselves to fully-virulent polio after it’d been attenuated down into a LAV – since the risks of improperly designing an experimental LAVs had been readily apparent for years, even all the way back then.
Even before today’s age of bespoke genetic engineering, live-attenuated vaccines were seen as extremely delicate and immunologically volatile. The slow unpredictable specter of deattenuation had already shown itself in that orphanage, however history would demonstrate that it wouldn’t be anywhere near enough horror to prevent the envelope from being pushed until the friction lit it on fire. In a few more decades, the profound and intense risks around attempting to splice the genes from an animal virus into Sabin’s perfectly-good OPV-LAV vaccine would trigger the Asilomar Conference, at which point the scientific community thought they had things under control - but more about that in just a few moments.
So to be fair, it took nearly three-quarters of a century after its initial design and implementation, until 2017, for Sabin’s OPV-LAV to deattenuate enough to create more new cases of polomyetis than natural polio, and even then it was only handfuls of each. In the meantime, untold millions were saved from debilitating paralysis, and the disease has been all-but eradicated except in these small pockets of deattenuated vaccine-derived polio virus (VDPV). Sabin’s protocol was invented to complement the existing approach which used an inactivated strain attenuated past the point of death, which provided broad protection but not as effectively as Sabin’s interwoven three live-but-neutralized-strains in the oral OPV protocol that took his name. His LAV was meant to be the last nail in Polio’s coffin: It provided a more effective vaccine to protect troops from a disease that thrived in crowded military conditions, and the public health community with the last tool they’d need to eradiate the virus.
However the paradoxical phenomenon of paralytic polomyetis reassembling itself within vaccinated populations has exploded since 2017, and by 2019 there were 176 cases of polomyetis derived from the OPV strain worldwide when only 33 had been seen the year prior, and outbreaks of poliomyelitis have recently been seen in Egypt, the Dominican Republic, Haiti, the Philippines, and Madagascar.
2.1 - Memories of virulence gone past.
This paradoxical ability, for attenuated viral strains to deattenuate back into their original fully-virulent parent strain – much like the T-1000 was able to mercurially reassemble itself in the sequel to The Terminator – can be explained by examining polio and other RNA viruses not as discrete linear genotypes transmitted on by discrete strains, but instead as quasispecies swarms of virions which carry distinct but complimentary sets of alleles, which work in concert in real-time to establish and expand infections. One of the first empirical changes that comes once you consider an RNA virus as a quasispecies swarm is that at any point in time, all the extant variants’ genomes form a collective probability cloud that serves as the smallest selective unit, as opposed to using individual virions or any single extant genome in a population, the classical approach.
This quasispecies viral swarming is an amorphous behavior that describes the search for fitness that occurs as each successive generation of the swarm produces wider spectra of mutations, with the term “quasispecies” specifically describing “distributions of non-identical but related genomes subjected to a continuous process of genetic variation, competition, and selection, and which act as a unit of selection.” Each of these distributions can be considered as overlapping clouds of allelic statistical possibilities, each of which represents the spectrum of mutations that can be expected to emerge within a set number of generations - so their ratios will be constantly changing over successive generations and in different settings.
This type of effect has just begun to be explored within the classical model, by quantifying the antigenic waves that shimmer across the surface of quasispecies swarms as they shift between the host populations, and using these measurements to indirectly measure the quasispecies swarm itself. These antigenic waves have been observed to shift between populations of viruses and host during the search for adaptation, and after intense mathematical analysis this model concludes that if an antigenic wave is transmitting itself to many different hosts all at once and spitting-off multiple “lineage speciations,” so the overall complexity of the quasispecies swarm is increasing, it’s likely to continually build on itself until either transmission stops or new variants fail to emerge.
However this field is in its infancy, and besides without fully sampling a COVID-19 infection to get a completely representative sample of its quasispecies infective swarm, it will be impossible to accurately calculate anything at all.
The linear model of virology that’s been classically used presents the illusion of control, it entirely ignores the reality that the process of sampling a virus from a live host and then isolating it within a Petri dish so it can be studied and quantified is an extremely rough and loose process. And there is evidence that today’s commonly used metagenomic tools are in fact missing many of the extant viral strains, since “the large proportion of low-frequency variants and their dynamic change in frequency (e.g., by comparing sequential samples from a virus replicating in cell culture or in a live host organism) currently being revealed by ultra-deep sequencing portray a level of complexity not contemplated in the concept of genetic polymorphism of population genetics, at least as classically formulated.”
So hopefully scientists trained in the classical model can be honest about the reality that the tools they’ve always used are incredibly rough and might well be missing some of the nuance going on. Unless each and every scientist out there can confidently state that nothing about how this pandemic has unfolded has surprised them.
2.2 – “We don’t need no water…”
With viruses replicating continually once a successful infection has set in and begun to smolder, the most-fit variant for a given tissue will predominate in that exact tissue when a sample is taken only from it. However, although only one variant will appear in the smoky quasispecies swarm infecting this tissue-type, the smoldering infection will be continually throwing off new variants which represent different points in the possible mutational spectrum – some of which will be better adapted to neighboring tissues, and others acting as accelerants for the predominate variant, and intensifying its virulence.
Granted, the temperatures involved are in far different ranges, but a recent pre-print demonstrates that SARS-CoV-2’s various strains’ spike-proteins’ ability to infect different types of cell tissue changes depending on the temperature, with far different virulence at about 91-degrees Fahrenheit than at about 99 degrees depending on the strain involved. And further adding to the novel coronavirus’s potential for immunological conflagration, is the the fact it’s able to replicate 10-times more efficiently than SARS-CoV in the average temperature encountered in our upper respiratory tracts.
The idea of different variants acting as accelerants isn’t commonly used, but it fits the language humans have historically used: Infections sparking up out of nowhere, and burning through populations, and diseases appearing suddenly from sinister gaseous miasmatic vapors. And it fits the picture presented by the overall biochemistry: Successful viral entry into a cell requires the same underlying chemical principles of entropy and heat exchange as sparking and maintaining a fire, where just like a fire: a viral infection will begin destroying its host to make more of itself. Also demonstrating that it works via immunological conflagration, SARS-CoV-2 appears to prefer to begin its infection in the relatively hospitable nasal cavities that can host infections at low temperatures, before different variants are produced which allow it to invade tissue deeper in the body which require variants able to infect and biochemically burn at hotter temperatures.
And just like one gas acting as an accelerant for another’s combustion can be modeled mathematically by looking at their relative binding tendencies to different elements and how they react at different concentrations, the mathematical inevitability of quasispecies swarms fully exploring their mutational spectrum and finding variants to fuel their spread isn’t any different. It’s only the language that varies, as the literature currently describes the positive selection from quasispecies variants resulting in “hitchhiking” between mutations on variants in the same swarm, the exact same concept as different variants and their mutations acting as accelerates for each other during gaseous chemical combustion.
So if this model was accurate, we’d expect the first notable beneficial mutation – D614G – to fit within it pretty well. And it turns out, this variant’s adaptive advantage in fact comes from handling the body’s chemical temperature more effectively, allowing quasispecies clouds hosting it to create a “hotter” infection.
Or in a more classical sense, quasispecies swarms likely depend on a sort of accidentally eusocial viral altruism to prosper. Variants don’t exist in a vacuum, they work with their close cousins to most-effectively invade new tissue-types, and so “internal interactions of cooperation or interference can be established in what has been called the social behavior of viral populations.”
As one study revealed, although its usually possible to identify a majority consensus sequences from a sample of hosts infected by COVID-19, the sample had a broad median variant count of 23, with nearly 250 different variants found in total. And considering that about half of the observed mutations thought to have a significant impact on gene expression and samples differing throughout the day even in the same organ system, as well as the fact that barely 2% of the minority variants were found to overlap at all between any two hosts - the inherently nebulous quasispecies swarming nature of SARS-CoV-2 begins to coalesce even more.
Finally, although it’s hasn’t been studied as much yet, this more combustion-based model turns the current models of viral fevers on its head – instead of fevers emerging as the body’s attempt to fight off the virus, fevers may be viruses’ way of allowing for infections to spread into different tissue types deeper in the body. And so although they may appear to reduce the ability of the first infecting low-temperature variant to occupy the nasal tissue where it usually lands, as this is happening variants which can infect warmer tissue are pushing their way deeper into the fevered body.
And with any virus, but especially with coronaviruses, it’s important to keep in mind that hidden within their large genomes are entire suites of accessory genes which only appear functional while actually living inside their hosts, in vivo, and whose function won’t be observable within the virtual environment in lab Petri dishes, in vitro: “the coronavirus group-specific genes are not essential for growth in cell culture but function in virus-host interactions.”
Incidentally, another paper attempting to immunize against that highly-airborne coronavirus goes on to explain that when an experimental spike-protein only vaccine was tried against a highly-airborne feline coronavirus - immunoglobulin was thrown out of wack and 80% of the kittens it was administered to died inside a month. But don’t worry, Big Pharma has crossed its collective fingers and is hoping really, really hard that this exact same phenomenon doesn’t occur at some point down the road within human populations vaccinated with a spike-protein only vaccine against our novel highly-airborne coronavirus.
But this effect can’t be expected to appear immediately with SARS-CoV-2, since like all deattenuating LAVs it won’t reach full virulence until it’s fully reconstituted itself back to its original full-strength form - an enigmatic process that’s explained below, and which is still ongoing as transmission events occur in their millions all across the Earth.
So although SARS-CoV-2 may not seem terribly virulent in its initial chronic stage yet, you should probably keep in mind that attenuating the LAV for Yellow Fever took hundreds of passages through five different types of cells - including those from monkeys, mice, and chickens - in a process invented about 100 years ago. Meaning this novel coronavirus likely has a very long way to go before it can reconstitute itself back to its original strongest viral swarm, since it almost certainly went through an even more extensive attenuation process involving cutting-edge modern virological technology developed over the intervening century.
And it’s worth taking a moment to point out that the Yellow Fever virus used for this attenuation wasn’t exactly a naturally occurring virus, it was the result of sending the highly-pathogenic “Asibi” Yellow Fever virus - with a 95% kill rate in monkeys - through serial passage, until a chimeric recombinant virus now called 17D, which presumably expresses a wide range of genes, was produced - ideal since those genes would provide the necessary signaling-flags for our immune system to target after it’s attenuated down into a LAV. Which is very close to what Ralph Baric was doing serially passaging SARS-like viruses at UNC to see which genes got swapped around, but more about that soon. And in the case of Sabin’s first LAV for Polio, that version of OPV required three different strains to get all of the necessary epitopes, or immunology signaling-flags, which accomplishes the same affect as an artificial chimera expressing all of those epitopes at once would.
Within their hosts in vivo, examining RNA viruses as quasispecies swarms reveals that “viral types and subtypes are just the ‘tip of the iceberg’ of a more profound and fundamental phenomenon: the continuous dynamics of mutant generation, competition, selection and random events which push viral quasispecies towards diversification.” However the complete nature of a quasispecies swarm will never be revealed inside of the petri dish, or any lab at all unless ethics rules are adjusted, since without a population of live hosts to transmit between, an RNA virus will never use the variant potential of its entire genome and reveal the full extent of its quasispecies swarming abilities.
So long as an RNA virus is able to find new hosts to infect and so can continue replicating, its quasispecies swarm won’t attenuate upon continual replication and new host introduction, and its mutational cloud will continue to grow in diversity as the swarm grows in variant-derived complexity. And as these quasispecies swarms get larger, by definition they also become more variegated, and eventually more virulent once transmission begins.
2.3 – Time for life to spark.
Avian influenzas don’t magically attenuate over time on crowded industrial poultry farms, they’re now ubiquitous and growing more virulent there because the population densities involved mean that the quasispecies swarms of the avian influenzas infecting them have an unlimited supply of hosts and so never stop mutating toward highly pathogenic states, where a 50% fatality rate can be a best-case scenario. In a sense there’s an immunological pressure that slowly begins to build after population densities become unnaturally high, until it explodes with the emergence of a highly pathogenic strain that burns through an entire farm, generally killing at least half the flock and sometimes all of it.
The passage of time is a critical concept in quasispecies viral swarming behavior, as with enough generations a single viral genome of every major class of RNA virus has been shown to eventually give rise to a distribution of possible mutants which represent variation that is not immediately apparent from its genome. Whereas genomes made from DNA carry much of the code for the variation that exists in a given population even though each and every individual does not express it in a given lifetime.
RNA viruses replicate constantly inside of their hosts and do not have episodic sexual exchanges like most DNA-based organisms, underlying the fundamental need to approach RNA viruses from the ongoing and amorphous quasispecies perspective which views their evolution as the shifting spectrum formed from ratios of alleles in competition and cooperation, more than the largely polarized expectations of the discrete haplotypes found with DNA heredity. In a broad sense, the behavior of a mutant cloud of 100 variants with a relatively narrow spectrum attempting to infect human tissue over the course of a day, would roughly represent the genetic activity of a tribe of several hundred people attempting to survive in their environment over the course of dozens of generations.
And in a sense, the process of mammalian fertilization can be seen as a short term and accentuated mutant swarm. Although only one gamete is required to fertilize the egg, it does not complete its journey alone and needs its motile brethren to deal with host immune defenses and act as cannon fodder. So although quasispecies swarms always have multiple extant variants inside any one host at a given time, and mammalian zygotes host just one DNA-based genome, a mammalian father producing multiple offspring is also diffusing his genome into a swarm of variants – the winner is just declared one generation at a time.
This fundamentally amorphous nature of RNA virus genomes means that the quasispecies approach invalidates the idea of a singular “wild type” isolate genome with one immutable nucleotide sequence described as the contagion at any one moment in time. Because under this approach, every RNA virus is by definition a swarming ever-changing mutant cloud of quasispecies virions, in part because “RNA viruses, whether replicating in changing or static environments, keep a sustained level of genetic heterogeneity that maintains their capacity to respond to constraints.” This results in a quantum uncertainty around exactly which section of the cloud is being observed at any one moment, a cloud which will be different the next time you sample it regardless of how representative you think the sample you first sampled was.
This more statistical and fundamentally quantum approach to exploring the evolution of RNA viruses was suggested by Francis Crick to Dr. Manfred Eigen over an otherwise uneventful breakfast in 1971, and seemed promising given the results already obtained by Sol Spiegelman and colleagues from serial transfer experiments of RNA taken from a virus that infects bacteria in a closed system, which demonstrated Darwinian behavior in vitro. Eigen applied a statistical framework to Darwin’s expectations, and formulated an origin of life that used the replication and adaptability of self-organizing macromolecules to argue that they may have served as something akin to proto-RNA.
With an apparent drive towards complexity and the ability to self-replicate, RNA viruses form quasispecies clouds or swarms which evolve towards a composition and a mutation rate that leads to the ratio of variants with various levels of fitness for adaptation to its host population, values that are subject to change as the living and variable ecosystem of individuals they are being hosted in itself changes. These early findings were reinforced about half a century later, when in 2021 nuanced experimentation on molecules composed of just a few repeating units, whose behavior was expected to mimic the chemical precursors of RNA and DNA, displayed the ability to undergo a quasi-selective process involving the selection of more stable and ordered elementary structures based on even the most miniscule selective pressures, accompanied by the overall reduction in randomness which would be expected from complexifying life.
It’s not proof, but the fundamentally quantum behavior underlying quasispecies swarms likely helped spark life itself. And this wouldn’t be the first-time quantum effects showed up in fundamental biological processes, as they’ve been identified as playing roles in a vast array of fundamental processes: photosynthesis, tadpole maturation, human smell, and avian navigation, and are beginning to show flickers within neurobiology as well as Sir Roger Penrose has proposed that human consciousness emerges from neural-anatomical structures with ability to host quantum behavior.
And so it shouldn’t come as a surprise to find a fundamental framework from physics making its way into some fundamental biology as well, as our understanding of the forces in play becomes more granular and the math more precise.
2.4 – The price of Original Sin.
Although quasispecies theory is framed within a world of infinite possible generations, this approach to viral population genomics examines a virus not as any one discrete immutable genome, but instead as nebulous and mercurial quantum clouds of variants looking to find the highest shared fitness among a given population of hosts, variants which are able to swarm together in search of the highest collective fitness, looking to burn hotter than the host can defend itself against in a perpetual immunological arms-race.
And as masterfully captured in the case of the OPV-LAV strains which are able to deattenuate back to fully virulent polio like the T-1000 merging from thousands of shattered bits back into a whole, RNA viruses also seem to carry a “memory” of this past peak fitness state which doesn’t fade with time, a memory they are able to use as a selective shortcut when looking for the most adaptive mutations back to their original state.
This apparent memory of past viral fitness, the ability for an RNA virus to reassemble itself into its fully virulent original full-strength viral V-1000 form, may have evolved as a counterbalance to Original Antigenic Sin, a form of defensive host immune memory which causes many vertebral immune systems to produce bespoke ancestral antibodies tailored to mount an immune defense against the original example of any given class of virus, even when a different species within the same class infects it.
The best example of this is the mercurial H1N1 influenza variant behind the 1918 Spanish Flu pandemic, which effectively formed the V-1000 godfather that gave birth to the 1957, 1968, and 2009 H1N1 pandemics that began in different regions of the world. Oddly, even though it is the most contemporary outbreak and is separated from the original H1N1 strain by nearly a century, the 2009 H1N1 strain is the only one that targets the same blood-based receptor signified by H1, as opposed to H2 or H3. As Original Antigenic Sin would predict:
“When the 2009 pandemic virus emerged in humans with a swine H1 HA gene descended from, and still closely related antigenically to, the 1918 pandemic virus, extensive cross-protection between the 2009 and 1918 pandemic viruses was demonstrated in experimental animals (12–16). Interestingly, 1918 virus-specific [antibody-producing] B-cell clones could also still be recovered from very elderly survivors 90 years after their exposure to that virus but before their exposure to the 2009 pandemic virus.”
And so, Original Antigenic Sin may be evolutionarily entangled with the quasispecies memory which appears to allow RNA viruses to return to full virulence much more quickly than they should statistically be able to, in the sense that they each may have evolved to counterbalance each other as organisms and their communities increased in complexity.
RNA viruses have demonstrated this V-1000 ability not just after vaccine attenuation, but following bottleneck events as well – so if a minority population of the quasispecies swarm is separated from the rest of the population when their shared host population is itself bottlenecked, and this subset of the quasispecies cloud doesn’t contain any examples of the original V-1000 fittest full-strength variant, quasispecies memory would allow this refugee cloud to quickly produce V-1000 variants. While Original Antigenic Sin would help protect older members of the host population who had been exposed to the V-1000 strain years ago, but who would face fresh exposure once this refugee swarm made its way back to full V-1000 strength.
Viral quasispecies have been observed to exhibit this sort of complimentary swarming behavior and the accompanying memory, which appears to allow an RNA virus to search for and find deattenuating mutations within cell cultures as variants are passaged across the full populational spectrum: Within individual hosts as different organ systems make better homes for discrete variants, across local populations of a few individuals, and nearly simultaneously across geographically disparate populations of hosts as well.
This scalable, fractal nature of this phenomenon was definitively illustrated during the 2017 influenza season by a study which observed the temporally parallel evolution of the exact same set of mutations among the variants competing within individual immunocompromised patients, fighting for selection among clusters of hosts, and emerging simultaneously across the entire globe as well. Additionally, no matter which scale is used, quasispecies behavior follows the Wright-Fisher expectations of selection-mutation equilibrium when allele frequencies are calculated - meaning they within the expected probability curves even when counted across generations - and should be considered a viable approach for examining the behavior of any RNA virus.
And the underlying fractal nature of the COVID-19 pandemic is starting to be explored as well, as researchers have noted the self-similarity underlying fractal patterns being shared by infections across different cities, and started to use the power-laws underlying fractal kinetics to anticipate more of the seemingly isolated and unpredictable outbreaks, which are really just the result of the quasispecies swarms beginning to coalesce within populations where infections have been smoldering for days or weeks already – the nature of COVID-19’s ability to spread asymptomatically by definition means that apparently isolated clusters of infections will emerge with fractal tendencies instead of the linear ones classical virology typically assumes.
So instead of the classical model’s assumptions of outbreaks progressing roughly linearly as one distinct variant outcompetes the last and then jumps from host to host, what’s really happening is something closer to the edges of the an ever-mutating Mandelbrot Set pushing up through the surface of a vast ocean of hosts - pandemics are a kaleidoscopic of variants emerging in disparate regions as the swarm explores new combinations of possibilities, not the linear progression of variant from one host to the next.
With the seasonal flu claiming roughly one-quarter to a half-million lives worldwide each and every year, creating one of the most predictable strains on public health efforts across the entire planet, and with SARS-CoV-2’s pandemic killing at least two-million in its first year in the course of infecting at least one-hundred million more and counting, while leaving many of those it doesn’t kill with nebulous constellations of insidious long-term side-effects – there may be no two viruses whose effects are so historically constant and immediately salient, but so unpredictably modeled and explained. Additionally, the 1918 Spanish Flu Pandemic stands as the single deadliest immunological event in recorded human history, claiming some 50 million victims, and drawing eerie parallels to today, when again an unusual airborne RNA virus has again emerged without any definitive source and created another global pandemic that has ebbed, but shown no sign of receding just yet.
And so, examining all RNA viruses, but especially the potentially pandemic seasonal influenza as well as SARS-CoV-2 and the COVID-19 Pandemic it’s causing within the quasispecies framework presents possible explanations for a litany of paradoxical and mercurial behaviors from each virus: The inexplicable appearance and sudden disappearance of the 1918 pandemic influenza, where the 2009 Swine Flu likely started, SARS-CoV-2’s burgeoning ability to evade our immune systems and vaccines, failures of influenza vaccine trials in naval settings as well as the failure of the FluMist vaccine which functioned more efficiently than an ATM for the researchers involved than anything else, the novel coronavirus’s emergent pattern of convergent epistatic mutations across continents, the near disappearance of the seasonal flu across much of the world in 2020, and other more subtle peculiarities demonstrated by each virus.
Beyond all that, the reason you probably haven’t heard of quasispecies swarms before is tied directly into the start of COVID-19’s ongoing pandemic, as well as the fact that every legacy media outlet on earth seems to simply be acting as stenographers for either one group of scientists who have been huffily insisting that a laboratory origin is a conspiracy theory, and as a public relations team for another group of “scientists” who are pretending to be indignant about the lack of a real investigation from the WHO – when the WHO’s been transparently serving as a mouthpiece of the CCP since January 2020 – while actively sidelining the seminal peer reviewed literature, and trying to make the scientists behind it disappear.
Which certainly has nothing to do the interest every intelligence nation on earth has on this virus, especially the French who helped design and build the Wuhan Institute of Virology and the Americans who pioneered the technology at the University of North Carolina under the supervision of Dr. Ralph Baric.
Because obviously pharmaceutical companies and the defense industry are very open about what they’re doing, and wouldn’t do things like influence photogenic and charismatic junior scientists to spin things a certain way while behaving with no regard for academic ethics, or recruit narcissistic media personalities to act like they understand science they have no fundamental grasp of or degrees in, all while cosplaying as a low-rent Iron-Man.
You’d think if Science was the goal, then if the scientist who was the literal architect of the database which every other scientist on the entire planet has spent the past 20 years using to compare the most minute difference between genomes – that if Science was the goal and he’d also been the lead author of the first peer-reviewed paper to examine a possible laboratory-engineered origin of SARS-CoV-2, then you’d have heard his name just once in the legacy media, right?
3. “Learning to swarm, but they ain’t got wings.”
Instead of viewing an infection as primarily caused by a singular genome or a discrete haplotype that is reliably reproduced and inherited, using quasispecies behavior to analyze RNA viruses means starting from the observation that they’re ubiquitously composed of mutant swarms of variants, which respond to host immune defenses nearly in real-time by intermittently producing virions with slightly altered genomes in each and every generation. Then a minority of those variants are quickly able to find the first immunological weaknesses, prove to be adaptive, and reach fixation if they provide enough of an advantage either in the current tissue-type, or in a neighboring one – often by complimenting the variants around them in ways that are impossible to anticipate until they happen.
At any given time following the moment that an infection’s first successful embers take hold within a tissue, every host will always be hosting multiple variants of any given strain of any given RNA virus - and so it’s highly imprecise and profoundly counterproductive to refer to any single host as being infected by just one variant’s genome, or even to the existence of a set “wild type” at any point in time in any given population. Depending on which organ is being sampled, and even what time of day it is – the composition of the quasispecies swarm is a shifting cloud of amorphous variability.
Even time itself clearly influences COVID-19 infections, as scientists have noted that infections appear to be twice as virulent around 2pm compared to the lowest times of day. One genome will often be in the majority within any major organ system across an entire population of relatively healthy non-immunocompromised hosts, so nations which only or primarily use nasal samples will erroneously conclude that one variant exists across an entire population, when dozens of other variants are hidden as minorities in other organ systems.
Sampling only noses will only reveal the dominate variant in nasal tissue, which will be shared across hosts in a population, even though multiple other variants will likely be present in other organ systems but not presenting in the nasal cavities. At any given time, the average host will have different slightly-altered variants of the same strain infecting each of their different organ systems, and so sampling nasal, pulmonary, intestinal, and fecal samples predictably demonstrates that after any meaningful amount of time each host will always be infected by multiple variants, especially once the infection spreads past the first type of tissue it infected.
This becomes the most apparent in immunocompromised patients who are also stricken with influenza, or those stricken with COVID-19 – both highly contagious respiratory RNA viruses with pandemic potential. In the case of COVID-19, although the popular press has presented the narrative that immunocompromised patients infected by the novel coronavirus are themselves creating new variants, a more granular analysis of their cases as well as those of immunocompromised influenza patients, makes it clear that because immunocompromised patients are mounting a weaker defense, each organ system is less able to constrain a mutant swarm to only produce the type of variant best suited for it – resulting in immunocompromised patients presenting as representative kaleidoscopes of the extant variants in a population. Curiously, the persistence of OPV live-vaccine strains in immunocompromised patients is also well-documented, where they produce the same kaleidoscope of variants and can use the same Terminator-like effect to reassemble themselves into a V-1000 form, what are called highly-diverged immunodeficient vaccine-derived polio viruses (iVDPVs).
And in crowded institutional settings like orphanages, these vaccine-derived V-1000 viruses are beginning to present the troubling problem of blocking the efficacy of existing vaccinations and innate immunity across the entire population. The emergence of these extraordinarily immune-evasive VDPVs are a stark reminder that a LAV going-wrong is just about the worst-case scenario as far as genetic experimentation goes. And strangely, the actual variola virus used for the production of the first viral LAV, which was attenuated to combat smallpox, has been lost to history just like the original “Asibi” Yellow Fever virus and its 17D derivative used to make the Yellow Fever LAV.
The practice of variolation, rubbing tissue from livestock infected with a virus related to smallpox onto humans to effectively vaccinate them, had been in practice throughout Asia for hundreds of years before it was finally industrialized for mass consumption by “The Father of Immunology,” Edward Jenner, in 1786.
Although the process or variolation, the earliest version of formal controlled vaccination, is usually explained by using cowpox’s close relationship to smallpox allowing it to accidently inoculate dairymaids against the later deadly disease, Jenner didn’t actually use cowpox to derive his live-attenuated vaccine.
We have no idea what he used.
3.1 – “We must rebuild us. We have the technology.”
The virus he did use is casually referred to as Variola in the literature, however no one actually knows precisely what it was. It wasn’t actually smallpox, it wasn’t cowpox, but it was over 99% similar to a bovine virus that also likely would’ve provided immunity against smallpox. However it’s important to note that even from the start, the creation of a live-attenuated virus will lead to strains whose ability to reassemble themselves into an original V-1000 form likely won’t be quite perfect, and in the case of iVDPVs the deattenuated strains appear more virulent and drug-resistant, and have the ability to interfere with existing immunity.
Healthy patients are able to mostly keep variants segregated within the organ systems they are most suited to, meaning that only pulling nasal samples from everyone can create the illusion that only one variant is circulating within a population, since the variant best suited for that tissue will generally be the most prevalent in that one tissue. On the other hand, immunocompromised patients are unable to enforce these barriers and the ratios of different variants created by them, and display all of the extant variants which due to less-effective immune systems, are able not only to spread between organ systems, but to replicate more evenly in each of them as well.
This can make it seem as if immunocompromised patients are producing new variants, when in fact all that is happening is that the ratios between variants are much more evenly represented among their organ systems, and so each variant more likely to show up in the sampling done of immunocompromised patients, which may often be more precise as well. Meaning immunocompromised patients only appear to host more variants, when in reality all that is likely happening is that the nature of their weakened immune systems makes it harder to keep variants segregated into each organ system, and so widespread testing of healthy individuals and their organ systems would reveal the same range of segregated variants that is in fact extant in the rest of the population, but which remains cryptic in everyone except in immunocompromised patients, whose organ systems are unable to keep variants segregated to each organ system.
Immunocompromised patients’ inability to keep variants segregated in their best-suited organ systems likely also plays a role in their relapses, as the quasispecies swarm can get greatly reduced in overall numbers with treatment, but as soon as weakness is sensed it will begin reconstituting itself. And especially bad news for immunocompromised patients is that diverse quasispecies swarms allow can allow viruses to pass through the blood-brain barrier and replicate inside the brain itself.
So immunocompromised patients are not necessarily producing more variants, however they can reliably serve as something of a fractal Rosetta Stones about the composition of the mutant cloud in the rest of the community, since their inability to constrain the infection leads to variants which will usually only thrive in one type of organ system in a healthy host being able to reproduce and thrive in many different organ systems. This was definitively shown in 2017 which used an immunosuppressed influenza patient and their community to demonstrate that the patient held a rough approximation of all the diversity found around him, with each variant roughly keeping to its best-fit organ system. And in the case of an airborne virus, becoming airborne in the first places appears to hinge on finding the proper mutations which allow it to colonize pulmonary tissue, where virions can be aspirated via coughing and sometimes even by just regular tidal breathing.
Due to the inherent complexity of balancing all of the competing and complimentary biological processes which they interact with, mutant swarms are by definition difficult to define exactly at any one moment in time, and so several variables must be considered at once when quantifying them. The five factors that regulating the formation of effective quasispecies swarms in RNA viruses are: “the average number of mutations per genome, virus population size, genome length, mutations needed for a phenotypic change, and virus fecundity.” And with virus population size, genome length, and virus fecundity all being some of the highest ever recorded in history for our novel coronavirus, three separate doors have been opened wide - allowing SARS-CoV-2 to establish extraordinarily robust quasispecies swarms all across the globe.
Additionally, despite the fact that SARS-CoV-2 began with an extremely efficient proofreading enzyme and a much lower mutation rate than polio and many other coronaviruses, the mutation rate regulated by that proofreading enzyme should be only one of five factors which should be considered when assessing quasispecies swarming behavior.
Beyond that, it appears that some of SARS-CoV-2’s non-structural proteins may quickly accumulate the in-frame deletions which by definition would not be caught by the proofreading enzyme at all, allowing it to cryptically mutate beyond the immune system’s surveillance. Or as the mayor of one Italian city racked by the virus described its behavior in general terms: “This is the demonstration that the virus has a sort of intelligence. We can put up all the barriers in the world and imagine that they work, but in the end, it adapts and penetrates them.”
And alarmingly, many signs point to the possibility that this not-so-friendly neighborhood novel coronavirus has already formed the robust and epigenetic quasispecies swarms which can allow variants isolated by bottlenecks as well as attenuated vaccine variants to remember past fitness states learned while part of an earlier swarm, since some kind of convergent evolution already appears to be occurring and “the same COVID-19 mutations are appearing in different places.”
This allows a hasty return to the peak virulence of their original V-1000 form through exposure to repeated hosts, since enough replication events will lead to a swarm of complimentary variants. This ability to learn and obtain a “memory” of a past fitter variant has been explored the most fully with OPV reverting back to virulent Polio by Dr. Adi Stern and his team at Tel Aviv University, but it has also emerged in Foot-and-Mouth Disease Virus (FMDV), and hepatitis C.
This paradoxical phenomenon seems to allow quasispecies swarms to find the most adaptive variants far more quickly than they should be able to statistically, and allows them to quickly remember how to neutralize host defenses, creating more virulent infections and viral mutant swarms which are much more dangerous – an interaction that has been playing out on poultry farms and during military vaccine trials for decades.
This apparent ability to have learned the most adaptive ratio of variants for a mutant swarm to effectively infect a host population and return to it is one of the hallmarks of quasispecies swarms, however the complete failure of the FluMist live-attenuated virus nasal vaccine at the community level, paradoxical results obtained from some military vaccine trials, and the difficulties of properly vaccinating poultry farms reflect another nebulous ability of quasispecies swarms that relies on the effects of quasispecies memory.
And it is one that, when combined with all of the implications of quasispecies viral memory, provides the best explanation for the origins and fates of both the 1918 Spanish Flu Pandemic as well as our current COVID-19 Pandemic.
4. The Golden Silkworm.
In ancient China, there was a tradition of developing a special poison called Gu by throwing as many venomous creatures as you could find into a jar and sealing them in, letting them kill each other in a knock-off zoonotic Thunderdome until only one was left. Also known as a “golden silkworm,” the lone surviving creature was then thought to host a “demonic poison” since every other creature’s venom was thought to be concentrated within it. According to Chinese folklore, this golden-silkworm could then mutate itself into any number of other animals – retaining its lethal ability no matter what form it took.
So it turns out that the concept of manipulating nature in an attempt to create unpredictable and unnaturally powerful weapons is nothing new. However, this ancient practice took a modern turn about 50 years ago, creating a threat to humanity that may have just reemerged from its container once more.
Back in 1977, a very peculiar epidemic began to sweep across Russia. Once scientists had isolated it, they discovered it was a rather unique strain of what’s come to be known as the H1N1 Swine Flu, a mutated variant of the virus that had caused the 1918 Spanish Flu Pandemic. That pandemic was caused by a flu with genes of avian origin, so it’s odd that this H1N1 variant was named a “Swine Flu,” right?
But since as the 1918 Pandemic was occurring scientists noticed it could jump into and kill pigs, they figured pigs had something to do with its origins, understandably since genomic sequencing wasn’t exactly readily available back then. Additionally, this particular variant of the H1N1 Swine Flu had something quite distinctive about its genome. And since it was so unique, going forward the H1N1 family will now be called the H1N1 Longpig Flu, which will make perfect sense in just a little bit.
At the time, the Soviet Union was employing tens of thousands of scientists designing every possible flavor of biological weapon, an expansive weapons program with a spotty safety record – pathogens were known to leak out of Soviet labs almost regularly. And Soviet scientists were reported to bring dead research animals home for dinner, meat was far from readily available in the USSR at that time, which parallels the reports of scientists in Wuhan smuggling dead lab animals out to sell for a few extra bucks on the street.
And as far as lab leaks go, China’s labs have leaked the SARS virus four times just in recent years. Even more specifically, a delegation from the State Department visited Wuhan’s Institute of Virology in early 2018 and asked for more resources for the lab since “the new lab has a serious shortage of appropriately trained technicians and investigators needed to safely operate this high-containment laboratory,” going on to emphasize how grave the consequences would be if a lethal virus managed to escape that lab.
So it’s probably important to consider that the original highly-pathogenic virus which SARS-CoV-2 was attenuated down from won’t be anything like any known or natural virus at all. Unlike rabies and Yellow Fever which can be isolated from wild animals in their highly-pathogenic state as they cause obvious illness, the process of forcing SARS-CoV-2’s original ancestor into a highly-pathogenic state - possible using a method close to the apocryphal golden silkworm involving feeding an endless supply of mammalian hosts to the virus to mimic the population density of poultry farms - would’ve created an entirely novel coronavirus unlike anything the world has ever seen.
And the very start of that process would like something like the experiments done at UNC, splicing difference viruses together to see what your new coronavirus chimeras might do.
4.1 – “Always keep the muzzle pointed in a safe direction.”
Lab leaks are nothing new for high-level virology labs across the world, and provide an avenue for COVID-19’s entrance onto the world stage that is just as viable as a natural zoonotic transmission – it isn’t and has never been a conspiracy theory. And leaks tend not to happen entirely randomly, the odds they occur are roughly paired with the pace of research into specific types of viruses.
For example, earlier in the 70’s before the Soviet H1N1 Longpig Flu leak, “the swine flu scare… [had] prompted the international community to reexamine their stocks of the latest previously circulating H1N1 strains to attempt to develop a vaccine,” which was seen to have increased the odds that someone, somewhere would make a mistake and leak an altered strain of the virus out of their lab. This increased pace of research mirrors recent times, when scientists have been investigating and trying to understand the supposedly impending threat posed by coronaviruses for years, capturing as many unique strains from the wild as they could, and mixing and matching their genomes in the lab.
In the years that followed the 1977 engineered leak, genetic analysis looking to determine where this particular strain of H1N1 Longpig Flu came from found something rather odd: It was very similar to strains of H1N1 that hadn’t been in circulation for decades, and seemed to be the product of “sequential passage in an animal reservoir,” which was determined since its genome seemed to be the combination of two strains, one of which hadn’t been in circulation for decades – making recombination in a laboratory the only plausible explanation beyond time travel. Curiously, although it seems to do almost everything else, COVID-19’s genome doesn’t appear to time-travel either, however it appears so distant from any related coronavirus that it’s been placed in its own clade, an isolated branch way out on its own in the viral family tree – meaning it’s the lone example of its kind, and doesn’t clump together with all the other known coronaviruses.
An increased pace of research into the H1N1 Longpig Flu back in the 1970s increased the odds that a mistake would happen until one eventually did, and a “leak” occurred. So maybe it’s worth keeping in mind that our current pandemic was preceded by years of research into coronaviruses everywhere from the University of North Carolina to the Wuhan Institute of Virology’s Disease Engineering Technical Research Center, and its related facilities.
And these capabilities have been further accelerated a massive push by the Chinese military to expand their biotechnological capabilities as well specific events like by a massive international conference meant to study a potential pandemic caused by a hyper-virulent strain of coronavirus, Johns Hopkins' Event 201. This international conference was funded primarily by the World Economic Forum as well as the Bill and Melinda Gates Foundation, and occurred in October 2019, just weeks before the nominal assumed start of COVID-19’s outbreak.
Leading up to 1977, an increased pace of research into strains of the flu was seen to increase the odds that an accidental leak would occur until one did - so shouldn’t the same logic should be applied to the start of our pandemic today?
Why is almost everyone today assuming that the increased pace of research means scientists anticipated this outbreak, instead of causing it? Wouldn’t an increased pace of research also increase the odds that a leak of a lab-modified coronavirus would occur, just like an increased pace of research precipitated the emergence of the engineered H1N1 Longpig Flu back in 1977?
4.2 – Nothing to see here.
The historical precedent of mysterious vaccine-like illnesses is that they are often linked to novel military-related vaccine programs, and their leaks are regularly covered up. For instance, the 1977 H1N1 Soviet Longpig Flu variant had been demonstrated as engineered, almost certainly by serial passage, by a paper in 1981, after every possible government denied any involvement at all for years.
And yet this paper remained hidden within the literature for 20 years, when after several months “arguing like two Jews over the last Torah,”1 Sirotkin & Sirotkin linked that paper definitively demonstrating an engineered origin to the modern discussion of gain-of-function engineering during the COVID-19 Pandemic, which is ongoing at the time of this writing.
Hopefully at the time of your reading right now it isn’t like a decade later, and this sucker’s still going strong. Man. Luckily, if there was any possibly at all for something as dystopian as that, surely everyone who had any information at all would be coming forward to help explain what’s going on. And that seems pretty much impossible, the virological community has circled their wagons and assured us that the idea of a lab being involved is either extraordinarily rare, or a conspiracy theory. Likewise, the academic intelligentsia has finally mustered the courage for some literary bukkake aimed at the WHO’s face, with an insipid letter pointing out well after one-hundred million infected and nearly three-million dead and a year has passed that a legitimate investigation needs to occur. Way to go, tigers – Team America World Police would be proud.
But Le Monde is the only newspaper or legacy media outlet on earth that has reported about or linked to the first and only peer reviewed paper which outlines how gain-of-function research may have played a role in the creation of both the virus itself and how it got subsequently got out of the lab. It highlights serial passage and its historical links to vaccine development and the mink’s close-cousin the ferret, and wasn’t written by any academic or research institution, or any of the scientists or institutions that’ve been involved with and profited from gain-of-function research for potential weapons or vaccine development. It was written by an ex-con and his dad and submitted in April of 2020, early enough to start a meaningful discussion that of course this thing might plausibly have escaped from a lab.
And it’s not like the link between ferrets and gain-of-function work is any secret, or hard to find if you’re a journalist even halfway trying to look:
“Although different animal models are used in vaccine studies, the most appropriate model for studying SARS is ferret since it develops the typical clinical signs, viral replication patterns and lung pathology compatible with that of SARS pathogenesis in humans.”
Because if the general public was aware that was legitimately on the table, it’s been demonstrated that public health measures would’ve been more easily followed. Plus there’s the common sense observation that it’s one thing to tell people to wear a mask because of some nebulous natural illness that doesn’t make most people all that sick, and quite another to tell them to wear a mask because this virus may effectively have been weaponized and we have no way at all to predict what its long-term effects might be or when it will take a turn for neurovirulence.
Wonder why that discussion never happened? A paper gets peer-reviewed and published, and then it’s almost like it doesn’t exist at all to the legacy media, or to the academic world which happily sidelines its existence and authors?
Take a moment to read just a snippet of his dad’s resume below, and compare that to the background of every talking head you currently see still on television having been demonstrably wrong for the past year and counting – almost all of whom have collected many thousands if not millions of dollars from some combination of the defense industry, the WHO, or pharmaceutical companies. Who would you trust?
My father contracted for a few months with one pharmaceutical company decades ago because his government salary didn’t seem like it’d be able to put two kids through college, other than that he has been a simple civil servant since he left the University of Tennessee after his second asshole kid broke his wife’s tailbone on the way out.
So why do you have no idea who this guy is, but see a regular parade of people telling you how okay it’s all about to be - all with completely public and often incredibly lucrative conflicts of interest, ever-present in the media, getting the science totally wrong and endangering you with their idiocy while they’re doing it? Why haven’t you heard from this guy?
“A 40 year PhD in Microbiology and designer of dbSNP, with nearly 20 years of molecular wet-work who'd previously taught molecular virology at the University of Tennessee and worked within the Theoretical Biology Division of the Los Alamos National Laboratory. At the time of his retirement from government service, he had more years working for GenBank than any other staff member - with his 28 years of service on the world's premiere DNA sequencing database making him one of the most experienced scientists on the planet when it comes to managing and analyzing genomic sequences.”
5. “You are not your fucking khakis.”
Unlike SARS-CoV-2, whose only encounter with humanity lead to an immediate global pandemic, small polio endemics have been plaguing humanity for millennia. However it has never established anything beyond endemic infections of less than 100,000 hosts at a time, and often far less than that. Far more profligate, SARS-CoV-2 instantaneously created a pandemic the moment it touched humanity, infecting over 100 million hosts in its first year by flashing across a world that is interconnected with international travel that has ebbed but not stopped throughout our pandemic. And although the functional impact of many mutations is still being determined, SARS-CoV-2 has already created a half-dozen distinct variants displaying difference vaccine sensitivities, transmissibility, and lethality - a number that only grows as surveillance is widened.
The nature of our interconnected planet as well as SARS-CoV-2’s ability for asymptomatic airborne transmission has created the possibility for quasispecies swarms, previously most closely studied infecting local endemic populations of hosts, to begin occurring on a much wider pandemic scale as they burn across humanity – as there is nothing to stop a variant in Buenos Aires from simultaneously emerging in Moscow, as several already have made that enigmatic genetic chorus across the globe.
The phenomenon of quasispecies viral swarming memory was starkly illustrated in vitro by Dr. Adi Stern from Tel Aviv University in 2017 using polio’s attenuated oral vaccine, OPV, as it worked its way back towards creating VDPVs.
The polio virus’s tendency for its once-virulent live-attenuated vaccine strains to find an accelerated evolutionary pathway back to virulence appears to be shared by other viruses and their LAVs as well, and in OPV’s case it appears that the first requirement is for three “gatekeeper” mutations to occur, which cause an increased replication rate in the variants carrying them. Curiously, although the experiments took place in tissue cultures lacking all the natural immunological pressure of a host’s full immune system and also the chance to recombine with endogenous viruses, four of the seven fitness-enhancing mutations were still found after passage through tissue culture:
“Interestingly, we discovered that the combinations of mutants were fitter than the sum of each mutant’s effect on its own, suggesting a synergistic epistatic interaction between all three mutations.”
And ever more noticeably, these gatekeeping mutations clearly violated the norms of expected evolutionary behavior, which makes intuitive sense when you consider that the process of attenuating a virus down through passaging is highly unnatural, so the return trip back to its original state would be equally unnatural on the way back :
“While past studies have assumed that parallel substitutions typically represent the fixation of positively selected mutations, the huge number of substitutions observed in parallel linages seems improbable and challenges this assumption. Instead we propose that several factors… lead to an unusual large number of parallel substitutions, which are not necessarily under positive selection.”
After these gatekeeper mutations have emerged and the reverting virus effectively passes through them, the next step usually involved recombination with an endogenous human hepatitis virus, however a functionally equivalent set of mutations conferred by recombination also emerged without any apparent recombination in some of the samples. Finally, a third wave of less predictable mutations would epistatically work together to slowly bring the once-attenuated OPV strain back to full virulence, where it could now establish the paralytic effects of poliomyelitis.
And, much like COVID-19 has established infections in immunocompromised patients which appear to pump out an unusually high number of variants, polio exhibits this exact same propensity, as do HIV and influenza, and many other classes of RNA virus - although this orderly gatekeeping has only been directly observed with reverting OPV so far.
In parallel to strains of SARS-CoV-2 from disparate parts of the world all exhibiting the same convergent and epistatic mutations despite having no apparent interaction with each other, OPV has done the same thing not just across geographic distance but across many years as well - in Egypt an OPV strain introduced in 1983 appears to have taken five years of circulation before it began to cryptically create active cases.
However with the COVID-19 Pandemic, it’s only taken about a year for scientists to notice that “the sequential increment of concurrent mutations from early lineages to descendent lineages as the pandemic unfolds still remains as an enigma,” in a study which also noted the appearance of epistatic gatekeeping mutations, as well as what appears to be a similar hierarchy of mutational development as deattenuating OPV. After a year of transmission, the authors noticed what appears to be a five-tiered hierarchy of evolution. Or as the Director of the UK’s Covid-19 Genomics Consortium observed, “Lots of mutations have just lit up almost at the same time, which is really fascinating.”
However perhaps this is due to bottlenecking in general and is simply a result of attempting to return to full V-1000 virulence in the form of a VDCV because of a natural environmental bottleneck, and not due to having originated in live-attenuated vaccine program?
How would we be able to tell the difference? But it sure would be weird if the exact same mutations all started to appear across several different species almost simultaneously, because that’s certainly not something the flu or any other human virus on earth has ever been observed to do.
Which is exactly what eventually began to happen, as not only does COVID-19 also display these coordinated, simultaneous, epistatic mutations across many different regions of the globe within human populations, these exact same mutations are also appearing in lab mice as well as on mink farms. There is absolutely nothing even vaguely approaching a natural parallel to this phenomenon, viruses do not use the same mutations to adapt to three different species simultaneously – different species require different mutations to establish active sustainable infections within a population, which is why diseases don’t just jump instantly and randomly between species, even ones living near each other.
So the fact that the exact same mutations which appeared in the UK and South Africa in humans, also appeared within the laboratory as SARS-CoV-2 was passaged through laboratory mice, is entirely unprecedented. And in mice, not only did repeated serial passaging make the same epistatic mutations that were seen in humans in the UK and South Africa appear, these mutations gave COVID-19 the ability to transmit through the air between the mice.
This kind of “gain-of-function” from serial passaging is a very direct sign of laboratory engineering, there is no natural way for the same mutations that cause a virus to become airborne between mice. would also show up simultaneously in a human population as well as mink, or the population of any other discrete species. Different species require different mutations for a virus to adapt to it and establish active infections, that is why zoonosis is such a big deal.
Although primarily a threat to poultry, Newcastle Disease has also been observed to reassemble itself and form active infections from attenuated vaccine strains, although this has been researched far less since it primarily infects chickens and poses no threat to human life. And classically, Marek’s disease has proved impossible to vaccinate against, as the attempts have all been “leaky,” and lead to a quasispecies swarm that’s one of the most virulent on earth - killing its hosts faster than Ebola kills humans, in just 10 days.
Another airborne viral disease, this one a coronavirus that also primary infects poultry named Infectious Bronchitis Virus (IBV), provides one of the best templates for transitioning from the classical view of “wild type” viruses to quasispecies swarms, as between any two strains of IBV, “only a few” amino-acid differences in their spike-proteins may lead to the establishment of a separate serotype, another obvious class of variants within the swarm that will need a vaccine that’s at least adjusted if not replaced entirely.
5.1 Symphisian swarms.
And as COVID-19 quasispecies swarm builds in complexity and new variants continue to emerge, perhaps scientists should keep in mind that when trying to vaccinate a poultry farm for IBV, another airborne respiratory coronavirus passing between crowded hosts, that often 10% of chickens fail to develop any protective immune response at all and that a less than 5% change in a strain’s spike-protein can lead to poor cross-protection. And this is with incredibly effective vaccines that target the virus’s entire genome, not just the spike-protein like our current experimental wave of mRNA vaccines.
So isn’t it strange that there’s no discussion at all about the issues controlling incredibly transmissible viruses on factory farms, even if they don’t threaten human life? After all, avian influenza infects most of the commercial poultry farms on earth at one time or another.
Now that’s an RNA virus that poses a threat to human life, as its quasispecies swarms are regularly able to produce the highly pathogenic variants which jump into farm-workers, despite the fact that poultry farms have spent decades running ubiquitous vaccination programs for their flocks which are carefully monitored and adjusted in the attempt to suppress the emergence of highly pathogenic variants. Poultry farms are under no illusion that they can ever come close to eradicating avian influenza on their farms given the extreme population densities involved, so their vaccine programs are designed to suppress the formation of the fittest highly pathogenic variants and test enough to catch and isolate the chickens which are inevitably infected with them.
Jam enough prospective hosts together in an industrial setting, add an airborne RNA virus that doesn’t create instant mortality in healthy hosts, set the conditions so that the virus spreads no matter what like on a chicken farm when the countless chickens just can’t help themselves from running around to keep on pecking their way up the order, and you don’t get herd immunity. You get a quasispecies swarm that spreads and grows in virulence continually, requiring continual surveillance and ongoing vaccination programs not to eradicate it – just to prevent its most lethal strains from forming. Strains which are evolutionary chomping at their bits to become more lethal and escape, as “one of the first observations derived from passaging viruses sequentially in cell culture was that when a virus was allowed to replicate at high multiplicity of infection (MOI) (high viral inoculum), the whole population tended to increase its fitness in an exponential manner.”
The additional bad news is that IBV arguably models SARS-CoV-2 far better than avian influenza, since both are within the same family of coronaviridae, and our COVID-19 Pandemic quickly seems to be spitting off the same sort of antibody-evading variants that IBV does as its quasispecies swarms grow, offering the same issues with vaccines – not to mention ones which only target the spike-protein as the mRNA vaccines currently do, since they don’t offer complete protection. After all, much like the military, “the poultry industry prefers to use live vaccines rather than inactivated ones. The former are cheaper to make and buy, and easier/cheaper to apply.”
And so in the case of COVID-19, its unusual asymptomatic spread made isolating infectious individuals impossible except in the most diligent nations, and so that element of ideal vaccination programs has been impossible for most of the world. But, luckily for humanity, a massive semi-collaborative international effort occurred to produce vaccines, including a brand new class of mRNA vaccine that skipped the final stage of animal testing because it was just so gosh-darn awesome. And so humans responded to a crisis the way we almost always do, applying our ingenuity to push back against yet another threat from nature, determined to impose our indomitable will one more time.
Because certainly, humans are smarter than chickens on poultry farms running around infecting and shitting all over each other, and humanity won’t end up in the same Sisyphean immunological cycle of never-ending illness and death. Weird that poultry farms made Soylent Green come true, and they’re actually fed each other’s carcasses.
Wonder if there’s a message there.
Kristin Sirotkin, 2020.